Correlation between polymorphisms of transforming growth factor-β1, tumor necrosis factor-related apoptosis-inducing ligand genes and nodular thyroid disease

2015 
Objective To study the correlation between individual gene polymorphisms of transforming growth factor (TGF)-β1 + 869 T/C, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) + 1525 G/A genes and nodular thyroid disease. Methods From September 2007 to December 2009, a total of 544 patients with nodular thyroid disease diagnosed in the Department of Endocrinology, The First Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology were selected, including 136 cases of nodular goiter patients (node group), 132 cases of thyroid tumor (adenoma group), 146 cases of Graves patients (GD group), and 130 cases of Hashimoto's thyroiditis (HT group). One hundred and thirty-five healthy subjects were enrolled as control group. Two milliliters of fasting venous blood of all subjects were collected. Polymorphisms of the TGF-β1 + 869 T/C and the TRAIL 1525 A/G genes were identified by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and the restriction fragment length polymorphism (PCR-RFLP) methods. Results TGF-β1 + 869 T/C: The CC genotypes and C allele frequencies of nodular goiter group[47.0%(64/136), 63.2%(172/272)] were significantly higher than those of normal control group [18.0% (22/135), 45.2% (122/270); χ2 = 30.76, 17.79, all P < 0.05]. The genotypes and allele frequencies of adenoma group[42.4% (56/132), 59.1% (156/264)] were significantly higher than those of the normal control group (χ2 = 24.40, 10.34, all P < 0.05). The risk of population carrying the C allele suffering from nodular goiter was 2.086 times of those carrying the T allele (OR = 2.086; 95% CI: 1.480-2.943). The risk of population carrying the C allele suffering from adenoma was 1.752 times of those carrying the T allele (OR = 1.752, 95% CI: 1.244-2.469). TRAIL + 1525 G/A: the genotypes and allele frequencies of nodular goiter group [40.4% (55/136), 62.9% (171/272)] were significantly higher than those of normal control group [12.0% (16/135), 48.5% (131/270); χ2 = 9.176, 11.307, all P < 0.05]. The genotypes and allele frequencies of adenoma group[53.3% (70/132), 73.1% (193/264)] were significantly higher than those of the normal control group (χ2 = 9.806, 33.82, all P < 0.05). The risk of population carrying the G allele suffering from nodular goiter was 1.796 times of those carrying the A allele (OR = 1.796, 95% CI: 1.275-2.531). The risk of population carrying the G allele suffering from adenoma was 2.884 times of those carrying the A allele (OR = 2.884, 95% CI: 2.009-4.142). Conclusions TGF-β1 + 869 T/C and TRAIL + 1525 G/A gene polymorphisms may be related to the incidence of nodular thyroid diseases; G allele of TRAIL and C allele of TGF-β1 may be predisposing genes of patients with nodular goiter. Key words: Transforming growth factor-β1; Tumor necrosis factor-related apoptosis-inducing ligand; Genes polymorphism; Nodular thyroid disease
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